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Enterochromaffin-like (ECL) cells and their growths: relationships to gastrin, reduced acid secretion and gastritis.
Baillieres Clin Gastroenterol. 1993 Mar; 7(1):149-65.BC

Abstract

ECL cells are argyrophilic endocrine cells of the stomach. Their distribution is species specific, however they are consistently located in the oxyntic mucosa and, in particular, in very close contact with the adenomeres of acidopeptic glands. ECL cells store histamine and are considered a key element in the mechanisms of gastric acid secretion as controlled by gastrin stimulus. Their peculiar anatomical disposition and secretory properties strongly suggest that ECL cells exert their function by a paracrine mechanism, i.e. by releasing histamine in the extracellular spaces surrounding acid-producing parietal cells. ECL cell activity is strongly stimulated by gastrin, which, once applied as a long-standing stimulus, also exerts a potent proliferating effect. Long-lasting hypergastrinaemia has been demonstrated to elicit ECL cell proliferation in laboratory animals, inducing ECL cell hyperplasia, dysplasia and ECL cell tumours, i.e. argyrophilic gastric carcinoids. However, in experimental rodents it is believed that hypergastrinaemia is not per se a stimulus capable of inducing ECL cell transformation, a predisposing genetic background being required for tumour development in endocrine organs. In man, long-standing hypergastrinaemia exerts the same proliferative pressure on ECL cells and is associated with hyperplasia with or without dysplastic changes and carcinoid development. Clinical evidence suggests that other factors, both genetic and environmental, are required to induce ECL cell transformation and carcinoid development. For this reason human gastric argyrophilic ECL carcinoids are subdivided into three main groups depending on their clinical background: (1) gastric carcinoids in patients with chronic atrophic gastritis; (2) gastric carcinoids in patients with Zollinger-Ellison and multiple endocrine neoplasia type 1 syndrome (MEN-ZES); and (3) solitary, sporadic gastric carcinoids. The clinical assessment of carcinoid-bearing patients is strongly recommended for better diagnosis and management of patients.

Authors+Show Affiliations

Surgical and Anatomical Pathology Service, IRCCS Policlinico San Matteo, Pavia, Italy.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

7682874

Citation

Solcia, E, et al. "Enterochromaffin-like (ECL) Cells and Their Growths: Relationships to Gastrin, Reduced Acid Secretion and Gastritis." Bailliere's Clinical Gastroenterology, vol. 7, no. 1, 1993, pp. 149-65.
Solcia E, Rindi G, Silini E, et al. Enterochromaffin-like (ECL) cells and their growths: relationships to gastrin, reduced acid secretion and gastritis. Baillieres Clin Gastroenterol. 1993;7(1):149-65.
Solcia, E., Rindi, G., Silini, E., & Villani, L. (1993). Enterochromaffin-like (ECL) cells and their growths: relationships to gastrin, reduced acid secretion and gastritis. Bailliere's Clinical Gastroenterology, 7(1), 149-65.
Solcia E, et al. Enterochromaffin-like (ECL) Cells and Their Growths: Relationships to Gastrin, Reduced Acid Secretion and Gastritis. Baillieres Clin Gastroenterol. 1993;7(1):149-65. PubMed PMID: 7682874.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Enterochromaffin-like (ECL) cells and their growths: relationships to gastrin, reduced acid secretion and gastritis. AU - Solcia,E, AU - Rindi,G, AU - Silini,E, AU - Villani,L, PY - 1993/3/1/pubmed PY - 1993/3/1/medline PY - 1993/3/1/entrez SP - 149 EP - 65 JF - Bailliere's clinical gastroenterology JO - Baillieres Clin. Gastroenterol. VL - 7 IS - 1 N2 - ECL cells are argyrophilic endocrine cells of the stomach. Their distribution is species specific, however they are consistently located in the oxyntic mucosa and, in particular, in very close contact with the adenomeres of acidopeptic glands. ECL cells store histamine and are considered a key element in the mechanisms of gastric acid secretion as controlled by gastrin stimulus. Their peculiar anatomical disposition and secretory properties strongly suggest that ECL cells exert their function by a paracrine mechanism, i.e. by releasing histamine in the extracellular spaces surrounding acid-producing parietal cells. ECL cell activity is strongly stimulated by gastrin, which, once applied as a long-standing stimulus, also exerts a potent proliferating effect. Long-lasting hypergastrinaemia has been demonstrated to elicit ECL cell proliferation in laboratory animals, inducing ECL cell hyperplasia, dysplasia and ECL cell tumours, i.e. argyrophilic gastric carcinoids. However, in experimental rodents it is believed that hypergastrinaemia is not per se a stimulus capable of inducing ECL cell transformation, a predisposing genetic background being required for tumour development in endocrine organs. In man, long-standing hypergastrinaemia exerts the same proliferative pressure on ECL cells and is associated with hyperplasia with or without dysplastic changes and carcinoid development. Clinical evidence suggests that other factors, both genetic and environmental, are required to induce ECL cell transformation and carcinoid development. For this reason human gastric argyrophilic ECL carcinoids are subdivided into three main groups depending on their clinical background: (1) gastric carcinoids in patients with chronic atrophic gastritis; (2) gastric carcinoids in patients with Zollinger-Ellison and multiple endocrine neoplasia type 1 syndrome (MEN-ZES); and (3) solitary, sporadic gastric carcinoids. The clinical assessment of carcinoid-bearing patients is strongly recommended for better diagnosis and management of patients. SN - 0950-3528 UR - https://www.unboundmedicine.com/medline/citation/7682874/Enterochromaffin_like__ECL__cells_and_their_growths:_relationships_to_gastrin_reduced_acid_secretion_and_gastritis_ DB - PRIME DP - Unbound Medicine ER -